KRAS and neoplasm: The TME can be categorized into immune, metabolic, microbial, and stromal subtypes.[13] These components engage in continuous cross‐talk and coevolved with tumor cells, significantly influencing drug response, toxicity, and resistance.[13, 14] There are both similarities and differences in the TMEs of tumors with wild‐type KRAS and those with KRAS mutations.[15] Comprehending the TME landscapes associated with KRAS variants and their inhibitors is crucial for precise TME regulation, representing the next frontier in the multi‐KRAS era.